Tanshinone IIa alleviates LPS-induced oxidative stress in dairy cow mammary epithelial cells by activating the Nrf2 signalling pathway

被引:8
|
作者
Fu, Kaiqiang [1 ]
Sun, Yuning [1 ,2 ]
Wang, Junbo [1 ]
Cao, Rongfeng [1 ]
机构
[1] Qingdao Agr Univ, Qingdao 266109, Shandong, Peoples R China
[2] Qingdao Hengxing Univ Sci & Technol, Qingdao, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Tanshinone IIa; Oxidative damage; Dairy cow; Nrf2; NF-KAPPA-B; MYOCARDIAL-INFARCTION; ANTIOXIDANT SYSTEM; LIPOPOLYSACCHARIDE; APOPTOSIS; SULFONATE; INFLAMMATION; EXPRESSION; RESPONSES; MASTITIS;
D O I
10.1016/j.rvsc.2022.08.008
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Objective: Mastitis is the most prevalent disease in dairy cows worldwide. Evidence has emerged that oxidative stress plays a crucial role in the development of mastitis. This study aimed to investigate the antioxidative effects of tanshinone IIa (Tan IIa) on LPS-induced oxidative stress in dairy cow mammary epithelial cells (CMECs).Methods and results: We examined the levels of ROS and MDA in LPS-treated CMECs after supplementation with Tan IIa using detection kits and found that Tan IIa significantly inhibited the upregulation of these factors. In addition, we also found that Tan IIa significantly reversed the decrease in mitochondrial membrane potential induced by LPS. Moreover, Tan IIa improved the activities of antioxidant enzymes, which were decreased by LPS. Finally, we examined the probable pathway in which Tan IIa exerted its antioxidant effects using qPCR and western blotting and found that Tan IIa significantly activated the Keap1/Nrf2 signalling pathway.Conclusion: These results suggest that Tan IIa might become a possible therapeutic agent for the treatment of dairy cow mastitis by weakening oxidative stress induced by LPS in CMECs.
引用
收藏
页码:149 / 155
页数:7
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